Effect of CD44 Aptamer on Snail Metastasis Factor and Aggressiveness of MDA-MB-231 Breast Cancer Cell Line

2020 ◽  
Vol 21 (5) ◽  
Author(s):  
Soudabeh Kavousipour ◽  
Pooneh Mokarram ◽  
Mahdi Barazesh ◽  
Elham Arabizadeh ◽  
Vahid Razban ◽  
...  

Background: The intracellular signaling pathways stimulated by CD44/hyaluronic acid (HA) interaction play a central role in the invasion and migration of cancer cells. Epithelial-mesenchyme transition (EMT) is an important factor in cancer metastasis and migration, which can be stimulated by the snail transcription factor. Previous studies showed cells that were subjected to snail-induced EMT, characterized by a CD44high/CD24low phenotype, expressed at their surface. Objectives: The aim of this study was to assess the inhibitory effect of CD44/HA interaction on the snail expression and invasive behavior of aggressive breast cancer cell line with a high CD44 expression in 2D and 3D culture. The cell surface binding capacity of the selected aptamer was evaluated via flow cytometry assay. Methods: To test our hypothesis, we disrupted the CD44/HA interaction by DNA aptamer, which specifically binds to the Hyaluronic Acid Binding Domain (HABD) of CD44. Then, expression level of snail mRNA was evaluated in MDA-MB 231 cells, cultured in 2D and 3D conditions by real-time PCR. Furthermore, invasive behavior was evaluated, using wound healing assay. Results: The results of this study showed that CD44 aptamer reduced snail expression and invasive behavior in MDA-MB 231 cell line. In addition, our result indicated that cells cultured in 3D were more sensitive to the aptamer in comparison to those cultured in the 2D model. Conclusions: The inhibition of CD44-HA interaction, using aptamer, negatively regulates the CD44 function in aggressive breast cancer cell line with the high level of CD44 expression.

2011 ◽  
Vol 131 (2) ◽  
pp. 276-286 ◽  
Author(s):  
Philip J. Medeiros ◽  
Baraa K. Al-Khazraji ◽  
Nicole M. Novielli ◽  
Lynne M. Postovit ◽  
Ann F. Chambers ◽  
...  

2013 ◽  
Vol 114 (6) ◽  
pp. 1385-1394 ◽  
Author(s):  
Katerina D. Fagan-Solis ◽  
Sallie Smith Schneider ◽  
Brian T. Pentecost ◽  
Brook A. Bentley ◽  
Christopher N. Otis ◽  
...  

2017 ◽  
Vol 10 (5) ◽  
Author(s):  
Bahareh Zarrin ◽  
Shaghayegh Haghjooy Javanmard ◽  
Fariba Samani ◽  
Mohamadhasan Tajadini ◽  
Maryam Jamady ◽  
...  

Drug Research ◽  
2020 ◽  
Vol 70 (10) ◽  
pp. 478-483
Author(s):  
Hamed Esmaeil Lashgarian ◽  
Vahid Adamii ◽  
Vajihe Ghorbanzadeh ◽  
Leila Chodari ◽  
Fayze Kamali ◽  
...  

Abstract Background Triple negative breast cancer is the most invasive breast cancer subtype and possesses poor prognosis and survival. Rho GTPase famil, especially Rac1 participates in a number of signaling events in cells with crucial roles in malignancy, migration and invasion of tumor cells. Silibinin, a flavonoid antioxidant from milk thistle has attracted attention in the recent decades for chemoprevention and chemotherapy of tumor cells. In this study, the effect of silibinin on the migration capacity of MDA-MB-231 cells, a highly metastatic human breast cancer cell line was investigated by evaluation of Rac1 expression. Method MTT wound healing and transwell assays were performed to evaluate the effects of silibinin on proliferation and migration of MDA-MB-231 cells. In addition, the influence of the silibinin on the expression of Rac1mRNAs was assessed by RT-PCR. Results Results indicated significant dose-dependent inhibitory effect of silibinin on proliferation and migration of MDA-MB-231 cells. It significantly inhibited the expression of Rac1 mRNA. Conclusion In conclusion, the results demonstrate that the silibinin can be used as an experimental therapeutic for the management of TNBC metastatic cancer.


2021 ◽  
Vol 14 (11) ◽  
Author(s):  
Mohammadreza Roshanazadeh ◽  
Hossein Babaahmadi Rezaei ◽  
Mojtaba Rashidi

Background: Cancer cell metastasis is facilitated by matrix-metalloproteinases through degradation of extracellular matrix (ECM) proteins and is a major cause of mortality. One of the most common remedies for cancer is chemotherapy, which has many side effects. Therefore, it seems necessary to find a way to reduce the side effects of these drugs while maintaining their anticancer effects. Quercetin (que) is a natural substance that has been reported to have anticancer activities. Objectives: This study aims at evaluating the effect of que in combination with doxorubicin (dox) on the migration of the MDA-MB-231 breast cancer cell line. Methods: The effects of que and dox on cell viability in 24h and 48 h was assessed by MTT assay. Also, the effects of the same drugs on the cancer cells migration were evaluated, using the wound healing assay. Lastly, the effects of que and dox were assessed on the expression of MMP-2 and MMP-9 genes. Results: The combination of 50 µM of que with 32 nM of dox was selected by CI comparison. The viability and migration of cancer cells and the gelatinases genes expression were decreased after treatment with individual drugs. The migration and the expression of MMP-2 and MMP-9 genes after treatment with the combination of que and dox was significantly reduced compared to the treatment with que and dox alone. Conclusions: Que inhibits the viability and migration of MDA-MB-231 cancer cells and synergistically enhances the effects of dox on the survival and migration of these cells. Hence, we propose this drug combination as a path for further research on breast cancer therapy.


2021 ◽  
Author(s):  
Maryana Teufelsbauer ◽  
Clemens Lang ◽  
Adelina Plangger ◽  
Barbara Rath ◽  
Doris Moser ◽  
...  

Abstract Metformin is used to treat patients with type 2 diabetes mellitus and was found to lower the incidence of cancer. Bone metastasis is a common complication of advanced breast cancer. The present study investigated the effects of metformin on human bone-derived mesenchymal stromal cells (BM-MSC) – breast cancer cell line interactions. BM-MSCs grown from box chisels were tested for growth-stimulating and migration-controlling activity on four breast cancer cell lines either untreated or after pretreatment with metformin. Growth stimulation was tested in MTT tests and migration in scratch assays. Furthermore, the expression of adipokines of BM-MSCs in response to metformin was assessed using Western blot arrays. Compared to breast cancer cell lines (3.6 ± 1.4% reduction of proliferation), 500 µM metformin significantly inhibited the proliferation of BM-MSC lines (12.3 ± 2.2 reduction). Pretreatment of BM-MSCs with metformin showed variable effects of the resulting conditioned media (CM) on breast cancer cell lines depending on the specific BM-MSC –cancer line combination. Metformin significantly impaired the migration of breast cancer cell lines MDA-MB-231 and MDA-MB-436 in response to CM of drug-pretreated BM-MSCs. Assessment of metformin-induced alterations in expression of adipokines by BM-MSC CM indicated increased osteogenic signaling and possibly impairment of metastasis. In conclusion, the anticancer activities of metformin are the result of a range of direct and indirect mechanisms that lower tumor proliferation and progression. A lower metformin-induced protumor activity of BM-MSCs in the bone microenvironment seem to contribute to the positive effects of the drug in selected breast cancer patients.


2014 ◽  
Vol 28 (3) ◽  
pp. 335-339 ◽  
Author(s):  
Kitson Liew ◽  
Phelim Voon Chen Yong ◽  
Yang Mooi Lim ◽  
Visweswaran Navaratnam ◽  
Anthony Siong Hock Ho

2017 ◽  
Vol 46 (3) ◽  
pp. 524-535 ◽  
Author(s):  
Seyede Elmira Yazdi Rouholamini ◽  
Saeid Moghassemi ◽  
Zahra Maharat ◽  
Amirhossien Hakamivala ◽  
Susan Kashanian ◽  
...  

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